Evidence of diet supplementation with vitamin C protecting honeybees from Imidacloprid induced peroxidative damage: a study with Apis cerana indica

Abstract

Neonicotinoids are one of the major stresses contributing to the decline in the population of honeybees. Worker bees are prone to various stress factors during foraging and are susceptible to Imidacloprid due to the reduction in the number of genes encoding for the major enzyme families responsible for the detoxification of toxins. The present study worked on the hypothesis that the dietary supplementation of Ascorbic acid (VIT C) could reduce the peroxidative damage in the worker bees of Apis cerana indica exposed to sub-lethal concentration of imidacloprid (IMD). Furthermore, we also evaluated the role and efficacy of VIT C supplementation on the cytoarchitecture of midgut tissues on exposure to IMD. Colonies of honeybees were maintained by providing sugar syrup to the control group and sugar syrup supplemented with 0.2% VIT C for the experimental group for six months. Worker bees from both groups were randomly collected and exposed to 0.001 mg/mL IMD. To study the peroxidative damage, the activities of various enzymes were analyzed. The activities of antioxidant enzymes including Catalase, Superoxide Dismutase, Glutathione S Transferase, and Glutathione Peroxidase in the hemolymph and midgut tissues of worker bees were significantly decreased due to exposure to IMD as a single agent. However, their activities showed a significant elevation under diet supplementation with VIT C. Histological examination revealed midgut tissue damage and the rupture of peritrophic membrane among the workers exposed to IMD as compared with the control group. The damage to the midgut was alleviated and the peritrophic membrane was found to be intact in the worker bees supplemented with VIT C. Our results indicated that the dietary supplementation of VIT C has the potential to maintain the redox status and thereby can offer protective potential against the peroxidative damages induced by the sub-lethal concentration of IMD.